Нетоз как фактор, способствующий развитию и прогрессированию сахарного диабета и его микрососудистых осложнений

Нетоз — новая форма гибели клеток — привлекает в последние годы пристальное внимание исследователей из-за его двойственного влияния на патологический процесс. Будучи изначально защитной реакцией врожденной иммунной защиты, направленной на улавливание и обезвреживание проникших в организм патогенов (бактерий, вирусов и грибов), нетоз при его чрезмерной активации может, напротив, способствовать прогрессированию заболевания, вызывая аутоиммунизацию, повреждение окружающей ткани или возникновение атеротромботических событий. В этом обзоре представлены данные о том, что образование в процессе нетоза внеклеточных ловушек нейтрофилов, называемых NETs, играет важную роль в патогенезе сахарного диабета (СД) и его микрососудистых осложнений. Например, при СД 1-го типа смерть β-клеток способствует секвестрации нейтрофилов в поджелудочную железу и четко коррелирует с увеличением нетоза. У пациентов с СД 2-го типа продукты высвобождения NETs также значительно повышены. Повышенный уровень дцДНК, маркера нетоза, коррелирует с развитием сердечно-сосудистых заболеваний и диабетической болезнью почек, что также согласуется со способствующей ролью нетоза в патогенезе таких диабетических осложнений, как нарушение заживления ран и диабетическая ретинопатия. Механизмы, связывающие нетоз с высоким уровнем глюкозы, не совсем понятны, поскольку нетоз повышен и у пациентов с диабетом, которые строго контролируют уровень глюкозы. Можно лишь предполагать, что нетоз не является следствием нарушения гликемического контроля, а, напротив, вызывает гипергликемию, которая в еще большей степени повышает исходно высокий уровень нетоза у пациентов с диабетом.

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